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1 Department of Physiology, University of Aarhus, DK-8000 Aarhus C, Denmark
* To whom correspondence should be addressed. E-mail: hgh{at}fi.au.dk.
We tested the hypothesis that increased Ca2+ uptake in rat extensor digitorum longus (EDL) muscle elicits cell membrane damage as assessed from the release of the intracellular enzyme lactate dehydrogenase (LDH). This was done using 1) electrical stimulation, 2) electroporation, and 3) a Ca2+ ionophore A23187. Continuous stimulation at 1 Hz for 120-240 min caused an increase in 45Ca uptake, which was closely correlated to LDH release. This LDH release increased markedly with temperature. After 120 min of electrical stimulation at 1 Hz, resting 45Ca uptake was increased 5.6-fold compared with unstimulated muscles. This was associated with an 8-fold increase in LDH leakage, an effect that was halved by lowering [Ca2+]o. The post-stimulatory increase in resting 45Ca uptake persisted for at least 120 min. An acute increase in sarcolemma leakiness induced by electroporation markedly increased 45Ca uptake and LDH leakage. Both effects depended on [Ca2+]o. The Ca2+ ionophore A23187 increased 45Ca uptake but caused no rise in tension. Concomitantly, LDH leakage increased 18-fold within 30 min, an effect that was abolished by omitting Ca2+ from the buffer. We conclude that increased Ca2+ influx may be an important cause of cell membrane damage arising during and after exercise or electrical shocks. Since membrane damage allows further influx of Ca2+, this results in positive feedback that may further increase membrane degeneration.
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